Evidence map›Paper›PMID 26455324›Full record

ArticleOncogene2016

Genome-wide screen identified let-7c/miR-99a/miR-125b regulating tumor progression and stem-like properties in cholangiocarcinoma.

K-Y Lin, H Ye, B-W Han, W-T Wang, P-P Wei, B He, X-J Li, Y-Q Chen

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
10.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.

  1. Molecular Targets and Signaling Pathways in Cholangiocarcinoma: A Systematic Review.Asian Pacific journal of cancer prevention : APJCP · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

K-Y LinKey Laboratory of Gene Engineering of the Ministry of Education, School of Life Science, State Key Laboratory for Biocontrol, Sun Yat-sen University, Guangzhou, China.
H YeDepartment of Hepatobiliary, and Department of Anesthesiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
B-W HanKey Laboratory of Gene Engineering of the Ministry of Education, School of Life Science, State Key Laboratory for Biocontrol, Sun Yat-sen University, Guangzhou, China.
W-T WangKey Laboratory of Gene Engineering of the Ministry of Education, School of Life Science, State Key Laboratory for Biocontrol, Sun Yat-sen University, Guangzhou, China.
P-P WeiKey Laboratory of Gene Engineering of the Ministry of Education, School of Life Science, State Key Laboratory for Biocontrol, Sun Yat-sen University, Guangzhou, China.
B HeDepartment of Hepatobiliary, and Department of Anesthesiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
X-J LiKey Laboratory of Gene Engineering of the Ministry of Education, School of Life Science, State Key Laboratory for Biocontrol, Sun Yat-sen University, Guangzhou, China.
Y-Q ChenKey Laboratory of Gene Engineering of the Ministry of Education, School of Life Science, State Key Laboratory for Biocontrol, Sun Yat-sen University, Guangzhou, China.
Sun Yat-sen University · CNSun Yat-sen Memorial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cholangiocarcinoma (CCA), which is a poor prognosis malignancy that arises from the malignant transformation of cholangiocytes, is associated with chronic inflammation of the biliary epithelium. Thus far, the molecular mechanisms of the origin and neoplastic processes of CCA that are promoted by inflammation are still unclear and need to be fully elucidated. Here using small RNA sequencing to determine the microRNA (miRNA) expression profiles in CCA, we found that let-7c, miR-99a and miR-125b, which are three miRNAs of the same cluster, were downregulated in CCA and targeted interleukin 6 (IL-6), IL-6R and type 1 insulin-like growth factor, which are important cytokines and receptors of the IL-6/signal transducer and activator 3 (STAT3) pathway and have key roles in inflammation and CCA initiation. We also found that enforced expression of let-7c, miR-99a or miR-125b could reduce the activity of STAT3 and further suppress CCA tumorigenicity in vivo and inhibit the migration and invasion of CCA cells in vitro. Surprisingly, let-7c/miR-99a/miR-125b cluster also significantly decreased the ability of CCA cells for cancer stem cell-like mammosphere generation by downregulating CD133 and CD44, which suggests the pivotal roles of let-7c, miR-99a and miR-125b in CCA by regulating both inflammation and stem-like properties. Our findings showed potential links between miRNAs and inflammation, and provide a potential treatment strategy for developing an miRNA-based therapy via IL-6/STAT3 targeting for CCA.

Indexed as

Gene Expression Regulation, NeoplasticAdultAgedAged, 80 and overAnimalsBile Duct NeoplasmsCell Line, TumorCholangiocarcinomaDisease ProgressionFemaleGenome-Wide Association StudyHEK293 CellsHumansInterleukin-6MaleMice, NudeIGF1R protein, humanIL6 protein, humanInterleukin-6MicroRNAsMIRN125 microRNA, humanMIRN99 microRNA, humanmirnlet7 microRNA, humanReceptor, IGF Type 1Receptors, Interleukin-6Receptors, SomatomedinSTAT3 Transcription Factor

Identifiers

PMID26455324
PMCPMC4932558
OpenAlexW2228056930

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.